Laryngeal cancer is detected commonly worldwide, and it ranks second highest in incidence among the respiratory tract neoplasms following only head and neck squamous cell cancer. In the present study salicin dimethyl ether was synthesized and evaluated against laryngeal cancers cells for anticancer property. MTT assay was used for the measurement of changes in TU686 and Tu212 cell proliferation while as induced apoptosis was detected by flow cytometry. Protein expression was determined by western blotting and expression of mRNA by RT-PCR assay. In the present study salicin dimethyl ether was synthesized by the reaction of salicin with methyl iodide using sodium hydride as base. Salicin dimethyl ether treatment led to a significant decrease in TU686 and Tu212 cell proliferation in a dose-dependent manner. In TU686 and Tu212 cells salicin dimethyl ether treatment caused a significant increase in cell apoptosis and elevated caspase-3 activity. Treatment with salicin dimethyl ether led to a prominent reduction in Bcl-2 protein expression in TU686 and Tu212 cells at 72 h. Salicin dimethyl ether treatment led to a prominent decrease in p-PI3K and p-Akt protein expression in TU686 and Tu212 cells, compared to the untreated cells. A significant increase in miR‑15a expression in TU686 and Tu212 cells was observed on treatment with salicin dimethyl ether at 72 h. In summary, the current study demonstrates that salicin dimethyl ether, a synthetic derivative of salicin, suppresses proliferation of TU686 and Tu212 cells. The underlying mechanism involves induction of apoptosis, inhibition of PI3K/Akt pathway and promotion of miR-15a expression. Therefore, salicin dimethyl ether may be used for inhibition of laryngeal cancer growth, however, in vivo studies need to be conducted to confirm the effect.
Background: Laryngeal squamous cell carcinoma (LSCC) is one of the most common forms of head and neck cancers. However, few studies have focused on the correlation between competing endogenous RNA (ceRNAs) and immune cells in LSCC.Methods: RNAseq expression of LSCC and adjacent tissues were downloaded from The Cancer Genome Atlas to establish a ceRNA network. The key gene in ceRNA was screened by the cox regression analysis to establish a prognostic risk assessment model. The CIBERSORT algorithm was then used to screen important tumor-infiltrating cells related to LSCC. Finally, co-expression analysis was applied to explore the relationship between key genes in the ceRNA network and tumor-infiltrating cells. The external datasets were used to validate critical biomarkers.Results: We constructed a prognostic risk assessment model of key genes in the ceRNA network. As it turned out, Kaplan-Meier survival analysis showed significant differences in overall survival rates between high-risk and low-risk groups (P < .001). The survival rate of the high-risk group was drastically lower than that of the low-risk group, and the AUC of 1 year, 3 years, and 5 years were all above 0.7. In addition, some immune infiltrating cells were also found to be related to LSCC. In the co-expression analysis, there is a negative correlation between plasma cells and TUBB3 (r = −0.33, P = .0013). External dataset validation also supports this result. Conclusion:In this study, we found that some key genes (SLC35C1, CLDN23, HOXB7, STC2, TMEM158, TNFRSF4, TUBB3) and immune cells (plasma cells) may correspond to the prognosis of LSCC.Abbreviations: ceRNA = competing endogenous RNA, DElncRNAs = differentially expressed lncRNAs, DEmRNAs = differentially expressed mRNAs, GEO = Gene Expression Omnibus, GO = Gene Ontology, HNSCC = head and neck squamous cell carcinoma, KEGG = Kyoto Encyclopedia of Genes and Genomes, LSCC = laryngeal squamous cell carcinoma, OS = overall survival, TCGA = The Cancer Genome Atlas.
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